Cardiomyopathy refers to diseases of the heart muscle. In cardiomyopathy, the heart muscle becomes enlarged, thick, or rigid. As cardiomyopathy worsens, the heart becomes weaker. It's less able to pump blood through the body and maintain a normal electrical rhythm. This can lead to heart failure or irregular heartbeats called arrhythmias. In turn, heart failure can cause fluid to build up in the lungs, ankles, feet, legs, or abdomen.
The Id1 and Id3 genes play major roles during cardiac development, despite their expression being confined to non-myocardial layers (endocardium-endothelium-epicardium). Animal models that lack Id1 and Id3 genes exist, and the cardiac phenotype is associated with ventricular septal defects, trabeculation and proliferation defects that result in a marked thinning of the myocardial wall. However, these animal models preclude the study of the roles of Id1 and Id3 in the postnatal heart, due to the lethality of the double knockout. As a result, the impact on the loss of vasculature on the postnatal heart is not known, and thus there is a lack of treatment options for cardiomyopathies associated with a thin myocardial wall. There is a need for new therapies to treat cardiac myopathies associated with the thinning of the myocardial wall.